Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease
Research of the human brain metabolism in vivo has largely focused on total glucose use (via fluorodeoxyglucose positron emission tomography) and, until recently, did not examine the use of glucose outside oxidative phosphorylation, which is known as aerobic glycolysis (AG). AG supports important fu...
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| Veröffentlicht in: | Neurobiology of aging 2018-07, Vol.67, p.95-98 |
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| creator | Vlassenko, Andrei G. Gordon, Brian A. Goyal, Manu S. Su, Yi Blazey, Tyler M. Durbin, Tony J. Couture, Lars E. Christensen, Jon J. Jafri, Hussain Morris, John C. Raichle, Marcus E. Benzinger, Tammie L.-S. |
| description | Research of the human brain metabolism in vivo has largely focused on total glucose use (via fluorodeoxyglucose positron emission tomography) and, until recently, did not examine the use of glucose outside oxidative phosphorylation, which is known as aerobic glycolysis (AG). AG supports important functions including biosynthesis and neuroprotection but decreases dramatically with aging. This multitracer positron emission tomography study evaluated the relationship between AG, total glucose use (CMRGlc), oxygen metabolism (CMRO2), tau, and amyloid deposition in 42 individuals, including those at preclinical and symptomatic stages of Alzheimer's disease. Our findings demonstrate that in individuals with amyloid burden, lower AG is associated with higher tau deposition. No such correlation was observed for CMRGlc or CMRO2. We suggest that aging-related loss of AG leading to decreased synaptic plasticity and neuroprotection may accelerate tauopathy in individuals with amyloid burden. Longitudinal AG and Alzheimer's disease pathology studies are needed to verify causality. |
| doi_str_mv | 10.1016/j.neurobiolaging.2018.03.014 |
| format | Article |
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AG supports important functions including biosynthesis and neuroprotection but decreases dramatically with aging. This multitracer positron emission tomography study evaluated the relationship between AG, total glucose use (CMRGlc), oxygen metabolism (CMRO2), tau, and amyloid deposition in 42 individuals, including those at preclinical and symptomatic stages of Alzheimer's disease. Our findings demonstrate that in individuals with amyloid burden, lower AG is associated with higher tau deposition. No such correlation was observed for CMRGlc or CMRO2. We suggest that aging-related loss of AG leading to decreased synaptic plasticity and neuroprotection may accelerate tauopathy in individuals with amyloid burden. Longitudinal AG and Alzheimer's disease pathology studies are needed to verify causality.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2018.03.014</identifier><identifier>PMID: 29655050</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aerobiosis ; Aged ; Aged, 80 and over ; Aging ; Aging - metabolism ; Alzheimer Disease - diagnostic imaging ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid imaging ; Amyloidogenic Proteins - metabolism ; Brain - diagnostic imaging ; Brain - metabolism ; Brain - pathology ; Brain aerobic glycolysis ; Cerebral metabolic rate of glucose ; Cerebral metabolic rate of oxygen ; Female ; Glucose - metabolism ; Glycolysis ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Neuronal Plasticity ; Oxygen Consumption ; Positron emission tomography ; Tau imaging ; tau Proteins - metabolism</subject><ispartof>Neurobiology of aging, 2018-07, Vol.67, p.95-98</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-7948e5a72c06844fe836eb3c64e429ab7b3ce422cd29acafacad5a0244c1ccb3</citedby><cites>FETCH-LOGICAL-c440t-7948e5a72c06844fe836eb3c64e429ab7b3ce422cd29acafacad5a0244c1ccb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197458018300927$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29655050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vlassenko, Andrei G.</creatorcontrib><creatorcontrib>Gordon, Brian A.</creatorcontrib><creatorcontrib>Goyal, Manu S.</creatorcontrib><creatorcontrib>Su, Yi</creatorcontrib><creatorcontrib>Blazey, Tyler M.</creatorcontrib><creatorcontrib>Durbin, Tony J.</creatorcontrib><creatorcontrib>Couture, Lars E.</creatorcontrib><creatorcontrib>Christensen, Jon J.</creatorcontrib><creatorcontrib>Jafri, Hussain</creatorcontrib><creatorcontrib>Morris, John C.</creatorcontrib><creatorcontrib>Raichle, Marcus E.</creatorcontrib><creatorcontrib>Benzinger, Tammie L.-S.</creatorcontrib><title>Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Research of the human brain metabolism in vivo has largely focused on total glucose use (via fluorodeoxyglucose positron emission tomography) and, until recently, did not examine the use of glucose outside oxidative phosphorylation, which is known as aerobic glycolysis (AG). AG supports important functions including biosynthesis and neuroprotection but decreases dramatically with aging. This multitracer positron emission tomography study evaluated the relationship between AG, total glucose use (CMRGlc), oxygen metabolism (CMRO2), tau, and amyloid deposition in 42 individuals, including those at preclinical and symptomatic stages of Alzheimer's disease. Our findings demonstrate that in individuals with amyloid burden, lower AG is associated with higher tau deposition. No such correlation was observed for CMRGlc or CMRO2. We suggest that aging-related loss of AG leading to decreased synaptic plasticity and neuroprotection may accelerate tauopathy in individuals with amyloid burden. Longitudinal AG and Alzheimer's disease pathology studies are needed to verify causality.</description><subject>Aerobiosis</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>Aging - metabolism</subject><subject>Alzheimer Disease - diagnostic imaging</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid imaging</subject><subject>Amyloidogenic Proteins - metabolism</subject><subject>Brain - diagnostic imaging</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain aerobic glycolysis</subject><subject>Cerebral metabolic rate of glucose</subject><subject>Cerebral metabolic rate of oxygen</subject><subject>Female</subject><subject>Glucose - metabolism</subject><subject>Glycolysis</subject><subject>Humans</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neuronal Plasticity</subject><subject>Oxygen Consumption</subject><subject>Positron emission tomography</subject><subject>Tau imaging</subject><subject>tau Proteins - metabolism</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9LAzEQxYMotla_guxB0Muuk91k_4CXUqwVCl56D9nsbE1JNzXZFeqnN6VV8OZhmDfw5g3zI-SOQkKB5o-bpMPB2VpbI9e6Wycp0DKBLAHKzsiYcl7GlFXFORkDrYqY8RJG5Mr7DQAUrMgvySitcs6Bw5gspnjIUtHa7JU1e699JLsm6uUQNbizXvfadpHuop1DZXSnlTTR1Hy9o96iu_dRoz1Kj9fkopXG482pT8hq_ryaLeLl28vrbLqMFWPQx0XFSuSySBXkJWMtllmOdaZyhiytZF0EHVSqmjAp2YZquISUMUWVqrMJeTjG7pz9GND3Yqu9QmNkh3bwIoWUZzSvsjxYn45W5az3Dluxc3or3V5QEAeUYiP-ohQHlAIyEVCG9dvTpaHeYvO7_MMuGOZHA4Z3PzU64ZXGTmGjA6peNFb_79I3FFGPLw</recordid><startdate>201807</startdate><enddate>201807</enddate><creator>Vlassenko, Andrei G.</creator><creator>Gordon, Brian A.</creator><creator>Goyal, Manu S.</creator><creator>Su, Yi</creator><creator>Blazey, Tyler M.</creator><creator>Durbin, Tony J.</creator><creator>Couture, Lars E.</creator><creator>Christensen, Jon J.</creator><creator>Jafri, Hussain</creator><creator>Morris, John C.</creator><creator>Raichle, Marcus E.</creator><creator>Benzinger, Tammie L.-S.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201807</creationdate><title>Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease</title><author>Vlassenko, Andrei G. ; 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| subjects | Aerobiosis Aged Aged, 80 and over Aging Aging - metabolism Alzheimer Disease - diagnostic imaging Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid imaging Amyloidogenic Proteins - metabolism Brain - diagnostic imaging Brain - metabolism Brain - pathology Brain aerobic glycolysis Cerebral metabolic rate of glucose Cerebral metabolic rate of oxygen Female Glucose - metabolism Glycolysis Humans Magnetic Resonance Imaging Male Middle Aged Neuronal Plasticity Oxygen Consumption Positron emission tomography Tau imaging tau Proteins - metabolism |
| title | Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease |
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